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Abstract

Objective

Astaxanthin (AST) is a carotenoid with anti-oxidative, anti-inflammatory, and anti-apoptotic properties. It
has also been reported that AST exerts protective effects against neurodegenerative diseases and reduces oxidative
stress-induced the central nervous system (CNS) injury. In this study, we aimed to evaluate the protective potential of
AST in inhibiting demyelination and oligodendrocyte death in a rat model of multiple sclerosis (MS).

Materials and Methods

In this experimental study, forty Wistar rats were randomly assigned to four experimental
groups: control group (with normal feeding), cuprizone (CPZ group) that daily received 0.6% CPZ for 4 weeks,
sham group that daily received 0.6% CPZ plus dimethyl sulfoxid (DMSO) for 4 weeks, and AST group that daily
received 0.6% CPZ and after 12 hours were treated with AST (3 mg/kg), for 4 weeks. Muscle strength was
evaluated by the behavioral basket test at the end of every week for 4 weeks. Luxol Fast Blue (LFB) staining
was utilized for the identification of myelination and demyelination. Myelin density was evaluated by the ImageJ
software. The expression of A2B5 (oligodendrocyte precursor protein) and myelin oligodendrocyte protein (MOG)
were assessed by immunohistochemistry (IHC) and the expression of myelin basic protein (MBP), MOG, and
platelet-derived growth factor-alpha (PDGFR-α) genes was examined by the real-time polymerase chain reaction
(RT-PCR) technique.

Results

The administration of AST reduced the oligodendrocyte damage and myelin sheath disruption in a rat model
of MS. The basket behavioral test showed the improvement of muscle strength in the AST group compared with CPZ
and sham groups. Besides, the results of real-time PCR and IHC indicated the beneficial effects of AST in declining
demyelination and oligodendrocyte death in a rat model of MS.

Conclusion

AST reduces damages to the myelin sheath and oligodendrocyte death in a rat model of MS.